Social isolation causes chemical changes in the brain
Experts at the California Institute of Technology have discovered a specific chemical that accumulates in the brain as a result of chronic social isolation. The researchers also found that this chemical is responsible for the negative effects of social isolation.
In humans, social isolation is linked to crippling mental health issues such as depression and post-traumatic stress disorder. Blocking the chemical buildup in the brain that results from seclusion could ultimately lead to a method of treating mental health disorders.
The research, which was conducted in the laboratory of David J. Anderson, was based on previous observations of social isolation in mice and the resulting behavioral changes.
In response to seclusion, mice show increased aggression, persistent fear, and hypersensitivity to threatening stimuli. For example, mice that have been socially isolated will remain frozen in place long after a potential threat has passed.
These effects are not seen as result of short-term isolation, suggesting that chronic isolation is what causes the changes in aggression and fear responses.
Previous research in the Anderson laboratory had uncovered a particular neurochemical called tachykinin that plays a role in promoting aggression in socially isolated flies.
Tachykinin is a neuropeptide that is released when certain neurons are activated. Neuropeptides alter the properties of other neurons when they bind to specific receptors, which has an impact on neural circuit function.
In mice, the tachykinin gene Tac2 encodes a neuropeptide called neurokinin B (NkB). Tac2 and NkB are produced by neurons in specific regions of a mouse’s brain – the amygdala and the hypothalamus – which are involved in emotional and social behavior.
The researchers found that chronic social isolation caused an increase in Tac2 gene expression and the production of NkB. When they administered a drug to chemically block NkB-specific receptors, the negative effects of isolation were eliminated and anxious mice began behaving normally.
The researchers also found that suppressing the Tac2 gene in the amygdala eliminated behaviors associated with fear, but not aggression. On the other hand, suppressing the gene in the hypothalamus eliminated increased aggression but not persistent fear. This finding indicates that various effects of social isolation are produced as Tac2 increases in different brain regions.
“The approach used here allowed us both to compare the effects of different manipulations of Tac2 signaling in the same brain region, as well as to compare the effects of the same manipulation across different brain regions,” said Anderson.
“The rich data set generated by these experiments revealed how this neuropeptide acts globally across the brain to coordinate diverse behavioral responses to social isolation stress.”
Study lead author Moriel Zelikowsky explained that humans have a signaling system comparable to the Tac2 system in mice, so this research may have potential applications for treating mental health disorders such as chronic stress.
“When looking at the treatment of mental health disorders, we traditionally focus on targeting broad neurotransmitter systems like serotonin and dopamine that circulate widely throughout the brain,” said Zelikowsky.
“Manipulating these systems broadly can lead to unwanted side effects. So, being able to precisely and locally modify a neuropeptide like Tac2 is a promising approach to mental health treatments.”
The study is published the journal Cell.